I've been trying to figure out WHY action potentials travel faster along a nerve cell when it has a myelinated sheath. It says on wikipedia that the sheath acts like a sort of insulator and dielectric (aren't dielectrics normally conductors though?). Now, a normal nerve cell is a capacitor, sitting at -70 mV when compared to the outside, if you add a myelin sheath, what will this do? It will decrease the potential difference, as an insulating dielectric such as the sheath will decrease the voltage difference for the same amount of charge, correct (it probably has a dielectric constant K < 1)?

Anyway, the way that the Na+ channels work in a cell is that a local equalization of potential in the cell will cause the Na+ channel in the area to shift upwards fully through the membrane, thus opening the channel (normally most of the protein is within the cell interior, attracted to the - ions inside).

Now, how exactly does the addition of the myelin sheath change this situation?

When the ions enter a myelinated axon through one of the nods of ranvier, there is obviously a current formation, but my question is, what are the physics behind the formation of that current? Why would an influx of ions suddenly start a current flow?

If you take away the myelin sheath, why would the current not flow?

Also, is it possible that a current is being propagated ALONG the dielectric? As the Na+ channels open at a node of Ranvier, the charge within the cell briefly rises to +40 or 50 mV. The dielectric on either side of it would no longer have a reason to be polarized it was before (- on the outside, + facing inwards), and would reverse configuration(+ on the outside, - on the inside), and this reversal would propogate along the sheath until hits the next node, thus depolarizing it.

I've always assumed that the sheathe confines the resting potential ions right next to the membrane, so when the gates open they flood through much faster (higher concentration leads to higher flux). The fact that the impulse travels faster between the nodes would seem to support that.

I like to think of it like so--from old school hole theory--with the un-myelinated portion I picture a fire bucket brigade, where one guy,or gal hands the bucket to the next person. This works but is slow. Now with the myelinated portion, the bucket person on the sending end now has to throw his bucket to the next person on the other side of the sheath. The person is strong enough to do so (potential energy) thus the bucket is thrown where the person on the other side of the sheath catches it. This works much faster, assuming no water is spilled. The key is potential energy, consider magnets, as you move one magnet closer to another there comes a point where the one magnet will just jump to the other.

Think of the myelin sheathe as a dense wrapping - this leaves a tiny space between the outside of the axon and the inside of the sheathe. Ions pumped into the space during the recovery phase are trapped there, right next to the membrane, in significantly higher concentrations than in an unmyelinated axon (or the Schwann cell gaps) - when an action potential opens the gates, the ions flow in much more quickly, depolarizing that part of the membrane and kicking open the next gates.

Remember, the impulse travels down the membrane, in a moving zone, gates opening at the front and shutting at the back. It's not jumping from gap to gap, it's just going faster where the wrapping is.

Darby wrote:Think of the myelin sheathe as a dense wrapping - this leaves a tiny space between the outside of the axon and the inside of the sheathe. Ions pumped into the space during the recovery phase are trapped there, right next to the membrane, in significantly higher concentrations than in an unmyelinated axon (or the Schwann cell gaps) - when an action potential opens the gates, the ions flow in much more quickly, depolarizing that part of the membrane and kicking open the next gates.

Remember, the impulse travels down the membrane, in a moving zone, gates opening at the front and shutting at the back. It's not jumping from gap to gap, it's just going faster where the wrapping is.

Ahh, so there are still a ton of voltage gated Na+ gates down the myelinated portion of the channel, it's just that these function a lot faster? That makes a lot more sense now, thanks! I hate the "jumping" explanation that low level courses give you, it's confusing

"Myelin is formed by specialized supporting cells called glial cells. Schwann cells myelinate axons in peripheral nerves and oligodendrocytes do so in the central nervous system. These glial cells wrap layer upon layer of their own plasma membrane in a tight spiral around the axon (Figure 11-30), thereby insulating the axonal membrane so that little current can leak across it. The myelin sheath is interrupted at regularly spaced nodes of Ranvier, where almost all the Na+ channels in the axon are concentrated. Because the ensheathed portions of the axonal membrane have excellent cable properties (in other words, they behave electrically much like well-designed underwater telegraph cables), a depolarization of the membrane at one node almost immediately spreads passively to the next node. Thus, an action potential propagates along a myelinated axon by jumping from node to node, a process called saltatory conduction. This type of conduction has two main advantages: action potentials travel faster, and metabolic energy is conserved because the active excitation is confined to the small regions of axonal plasma membrane at nodes of Ranvier."

Specifically the part where it says active excitation is confined... Doesn't this mean no leak channels are opening in the middle of the myelinated portion?